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Cancer pathogenesis and therapy

Pub Date : 2025-08-29 DOI: 10.1016/S2949-7132(25)00084-9

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Exploring marine-derived compounds as potential anti-cancer agents: Mechanisms and therapeutic implications 探索海洋衍生化合物作为潜在的抗癌剂：机制和治疗意义

IF 2.8

Cancer pathogenesis and therapy

Pub Date : 2025-08-26 DOI: 10.1016/j.cpt.2025.08.004

Nagaraju Bandaru , Yash Pramod Patil , Sumit Dilip Ekghara , Kunal Sharad patil , Mohan Gandhi Bonthu

Marine-derived compounds have emerged as a promising frontier in cancer research due to their remarkable structural diversity and broad-spectrum bioactivities. The marine environment, encompassing diverse organisms (e.g., sponges, algae, tunicates, mollusks, and marine microbes), is a prolific source of novel bioactive molecules with potent anti-cancer properties. Key classes of these compounds include alkaloids, polysaccharides, peptides, terpenoids, and polyketides, which exert anti-tumor effects through diverse mechanisms, including the induction of apoptosis, inhibition of angiogenesis, modulation of immune responses, interference with cell cycle progression, and targeting of critical signaling pathways involved in tumorigenesis and metastasis. Notably, marine-derived drugs such as trabectedin, eribulin, and plitidepsin have received regulatory approval for the treatment of various malignancies, demonstrating the translational potential of these natural compounds. Ongoing clinical and preclinical investigations are exploring a wide range of marine metabolites for their cytotoxic, anti-proliferative, and chemosensitizing properties. Advances in marine biotechnology, including genome mining, synthetic biology, and fermentation technologies, have significantly facilitated the discovery, sustainable production, and structural optimization of marine natural products. However, challenges such as low yield, structural complexity, limited water solubility, and poor bioavailability hinder their broader clinical application. The integration of novel drug delivery systems, such as nanoparticles, liposomes, and conjugates, offers a viable solution to overcome these limitations and improve pharmacokinetic profiles. This review provides a comprehensive overview of the mechanisms of action, therapeutic applications, and clinical development of marine-derived anti-cancer compounds. It also emphasizes the need for deeper insights into their molecular targets and the potential for synergistic use with existing chemotherapeutic agents. Future directions should focus on exploring untapped marine biodiversity, developing eco-friendly harvesting strategies, and developing innovative delivery platforms to fully harness the therapeutic promise of the marine pharmacopeia in oncology.

海洋来源的化合物由于其显著的结构多样性和广谱生物活性而成为癌症研究的一个有前途的前沿。海洋环境包括多种生物（如海绵、藻类、被囊动物、软体动物和海洋微生物），是具有有效抗癌特性的新型生物活性分子的丰富来源。这些化合物的关键类别包括生物碱、多糖、多肽、萜类和多酮类，它们通过多种机制发挥抗肿瘤作用，包括诱导细胞凋亡、抑制血管生成、调节免疫反应、干扰细胞周期进程，以及靶向肿瘤发生和转移的关键信号通路。值得注意的是，海洋衍生药物如trabectedin、eribulin和plitidepsin已获得监管机构批准，可用于治疗各种恶性肿瘤，证明了这些天然化合物的转化潜力。正在进行的临床和临床前研究正在探索广泛的海洋代谢物的细胞毒性、抗增殖和化学致敏特性。海洋生物技术的进步，包括基因组挖掘、合成生物学和发酵技术，极大地促进了海洋天然产物的发现、可持续生产和结构优化。然而，产率低、结构复杂、水溶性有限和生物利用度差等挑战阻碍了它们更广泛的临床应用。新型药物传递系统的整合，如纳米颗粒、脂质体和缀合物，为克服这些限制和改善药代动力学特征提供了可行的解决方案。本文综述了海洋来源的抗癌化合物的作用机制、治疗应用和临床研究进展。它还强调需要更深入地了解它们的分子靶点以及与现有化疗药物协同使用的潜力。未来的方向应该集中在探索尚未开发的海洋生物多样性，开发生态友好的收获策略，开发创新的输送平台，以充分利用海洋药典在肿瘤学中的治疗前景。

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引用次数: 0

C-X-C chemokine receptor type 4 (CXCR4) antagonism in precision oncology: Clinical applications and future directions C-X-C趋化因子受体4型（CXCR4）拮抗剂在精准肿瘤学中的临床应用及未来发展方向

IF 2.8

Cancer pathogenesis and therapy

Pub Date : 2025-08-22 DOI: 10.1016/j.cpt.2025.08.003

Aswini Rajendran, Veronica Elumalai, Saranya Balasubramaniyam, Karthikeyan Elumalai

Physiologically, the C-X-C chemokine receptor type 4 (CXCR4) signalling pathway regulates key aspects of tumor behavior (growth, metastasis, and immune evasion) and modulates immune system function. Anticancer researchers have identified peptide-based CXCR4 antagonists as promising candidates due to their high targeting specificity and favorable safety profiles. This review provides an analytical examination of CXCR4 antagonistic peptides,the selective Mavorixafor (X4P-001), an advanced, selective CXCR4 inhibitor. When Mavorixafor binds to the same location as C-X-C motif chemokine ligand 12 (CXCL12), it disrupts the CXCR4 protein receptor, stopping signals that help cancer grow and spread, as well as the formation of new blood vessels. Mavorixafor blocks cancer cell progression and metastatic growth in different tumor models while enhancing chemotherapy, radiotherapy, and immune checkpoint inhibitor efficacy. Antagonistic peptides AMD3100 (Plerixafor), LY2510924, and POL6326, as well as their therapeutic potential. Mavorixafor is a promising option for cancer treatments that combine different therapies because it stays attached to its target for a long time and can be taken by mouth. Clinical studies have demonstrated that Mavorixafor produces promising outcomes when combined with chemotherapy or immune checkpoint inhibitors during the treatment of both hematological malignancies and solid tumors. Mavorixafor is promising for cancer treatment because it works well with other therapies, such as immune checkpoint inhibitors and chemotherapy, as well as targeted therapies and radiation therapy. Future research on Mavorixafor will focus on two main areas: personalized medicine development, new delivery systems and their broad medical applications extending beyond oncology. As a potential CXCR4 antagonist, Mavorixafor shows promise as a transformative tool in cancer care because it regulates the tumor microenvironment (TME) while increasing the degree of therapeutic benefits.

生理上，C-X-C趋化因子受体4型（CXCR4）信号通路调节肿瘤行为（生长、转移和免疫逃避）的关键方面并调节免疫系统功能。抗癌研究人员已经确定了基于肽的CXCR4拮抗剂作为有希望的候选药物，因为它们具有高靶向特异性和良好的安全性。本文综述了CXCR4拮抗肽的分析研究，选择性的Mavorixafor (X4P-001)，一种先进的，选择性的CXCR4抑制剂。当Mavorixafor结合到与C-X-C基序趋化因子配体12 （CXCL12）相同的位置时，它会破坏CXCR4蛋白受体，阻止帮助癌症生长和扩散的信号，以及新血管的形成。Mavorixafor在不同肿瘤模型中阻断癌细胞进展和转移生长，同时增强化疗、放疗和免疫检查点抑制剂的疗效。拮抗肽AMD3100 (Plerixafor)， LY2510924和POL6326，及其治疗潜力。Mavorixafor是一种很有前途的癌症治疗选择，它可以结合不同的治疗方法，因为它可以长时间附着在目标上，并且可以口服。临床研究表明，在血液系统恶性肿瘤和实体肿瘤的治疗中，Mavorixafor与化疗或免疫检查点抑制剂联合使用产生了很好的结果。Mavorixafor很有希望用于癌症治疗，因为它与其他疗法（如免疫检查点抑制剂和化疗）以及靶向治疗和放射治疗效果良好。未来对Mavorixafor的研究将集中在两个主要领域：个性化医疗开发、新的给药系统及其在肿瘤学以外的广泛医疗应用。作为一种潜在的CXCR4拮抗剂，Mavorixafor在提高治疗效益的同时调节肿瘤微环境（TME），因此有望成为癌症治疗的变革性工具。

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引用次数: 0

Investigating hypoxia-inducible factor signaling in cancer: Mechanisms, clinical implications, targeted therapeutic strategies, and resistance 研究癌症中的缺氧诱导因子信号：机制、临床意义、靶向治疗策略和耐药性

IF 2.8

Cancer pathogenesis and therapy

Pub Date : 2025-07-12 DOI: 10.1016/j.cpt.2025.07.003

Abdul Halim Shaikat , S.M. Asadul Karim Azad , Md Azizur Rahman Tamim , Mohammed Sailim Ullah , Mohammad Nurul Amin , Mofazzal K. Sabbir , Md Towhidul Islam Tarun , Md Saqline Mostaq , Shohana Sabrin , Md Zihad Mahmud , Md Ashiq Mahmud

Hypoxia, a hallmark of the tumor microenvironment (TME), drives cancer progression through immune modulation, angiogenesis promotion, metabolic reprogramming, and uncontrolled cell proliferation. This review explores the diverse functions of hypoxia-inducible factor (HIF) signaling in cancer development and progression, providing a comprehensive overview of the molecular pathways. HIFs, particularly HIF-1α and HIF-2α, regulate several genes related to cancer hallmarks such as invasion, metabolic reprogramming, angiogenesis, and therapy resistance, thus mediating a significant portion of the hypoxic response. Hydroxylation of proline and asparagine residues in HIF-α subunits, which occurs in an oxygen-dependent manner, serves as a key regulatory mechanism for both their stability and transcriptional function. Notably, this complex interaction is regulated by multiple signaling pathways, including the extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK), phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR), and Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways. In cancer, HIF signaling affects several aspects of tumor cell biology that contribute to the cancerous characteristics, including angiogenesis induction through the upregulation of vascular endothelial growth factor (VEGF) expression, metabolic reprogramming through the enhancement of the Warburg effect, facilitation of cancer invasion and metastasis by driving epithelial-to-mesenchymal transition (EMT) and matrix remodeling patterns, and mediation of therapeutic resistance partly due to the effects on drug efflux pumps and DNA damage repair. Direct and indirect HIF inhibitors—including small molecules, peptidomimetics, antibodies, and proteolysis-targeting chimeras (PROTACs)—are under preclinical and clinical evaluation for their therapeutic efficacy. Preclinical and early clinical trials have demonstrated significant synergistic effects in inhibiting tumor development when HIF inhibition is combined with traditional therapies (chemotherapy or radiation) or immunotherapies, emphasizing major clinical implications and the potential for improving patient outcomes. Although challenges exist, particularly regarding drug resistance, further research to improve therapeutic efficacy and prolong survival for patients is warranted.

缺氧是肿瘤微环境（TME）的标志，通过免疫调节、血管生成促进、代谢重编程和不受控制的细胞增殖驱动癌症进展。本文综述了缺氧诱导因子（HIF）信号在癌症发生和发展中的多种功能，并对其分子通路进行了全面的综述。hif，特别是HIF-1α和HIF-2α，调节与癌症特征相关的几个基因，如侵袭、代谢重编程、血管生成和治疗抵抗，因此介导了缺氧反应的重要部分。HIF-α亚基中脯氨酸和天冬酰胺残基的羟基化以氧依赖的方式发生，是其稳定性和转录功能的关键调控机制。值得注意的是，这种复杂的相互作用受到多种信号通路的调节，包括细胞外信号调节激酶/丝裂原活化蛋白激酶（ERK/MAPK）、磷酸肌苷3-激酶/蛋白激酶B/雷帕霉素机制靶点（PI3K/Akt/mTOR）和Janus激酶/信号转导和转录激活因子（JAK/STAT）通路。在癌症中，HIF信号影响肿瘤细胞生物学的几个方面，这些方面有助于癌症特征，包括通过上调血管内皮生长因子（VEGF）表达诱导血管生成，通过增强Warburg效应促进代谢重编程，通过驱动上皮-间质转化（EMT）和基质重塑模式促进癌症侵袭和转移。以及部分由于药物外排泵和DNA损伤修复的影响而介导的治疗抗性。直接和间接的HIF抑制剂——包括小分子、肽模拟物、抗体和靶向蛋白水解嵌合体（PROTACs）——正在临床前和临床评估其治疗效果。临床前和早期临床试验表明，当HIF抑制与传统疗法（化疗或放疗）或免疫疗法联合使用时，在抑制肿瘤发展方面具有显著的协同作用，强调了主要的临床意义和改善患者预后的潜力。尽管存在挑战，特别是在耐药性方面，但有必要进一步研究以提高治疗效果并延长患者的生存期。

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引用次数: 0

Improving research transparency: An interpretation of the updated consolidated standards of reporting trials 2025 guideline from the perspective of clinical trials in oncology 提高研究透明度：从肿瘤学临床试验的角度解读最新的综合试验报告标准2025指南

IF 2.8

Cancer pathogenesis and therapy

Pub Date : 2025-07-08 DOI: 10.1016/j.cpt.2025.07.002

Yaguang Peng , Peng Lyu , Xiaoxia Peng

引用次数: 0

Neuroendocrine prostate cancer (NEPC)-associated CEP55 promotes cisplatin resistance in prostate cancer by regulating CDK1 phosphorylation 神经内分泌前列腺癌（NEPC）相关的CEP55通过调节CDK1磷酸化促进前列腺癌的顺铂耐药

IF 2.8

Cancer pathogenesis and therapy

Pub Date : 2025-07-05 DOI: 10.1016/j.cpt.2025.06.008

Zhuocheng Lai , Chenxi Hu , Jirong Jie , Yongyuan Xiao , Yuanchao Zhu , Xueni Guo , Yintong Liu , Yiwei Wang , Shiyu Pang , Xiangbo Zeng , Wanlong Tan , Qiong Wang

Neuroendocrine prostate cancer (NEPC) is an aggressive subtype of castration-resistant prostate cancer (CRPC) that is typically resistant to nearly all current therapies. In this study, single-cell RNA sequencing (scRNA-seq) and dataset analyses identified Centrosomal Protein 55 (CEP55) as a critical factor in the transformation from hormone-sensitive prostate cancer (HSPC) to CRPC and, ultimately to, NEPC. Subsequent bioinformatics analyses and validation with clinical samples demonstrated that CEP55 is significantly upregulated in NEPC tissues compared to HSPC and CRPC. Furthermore, while CEP55 show no significant association with the immune microenvironment or cancer-associated fibroblasts (CAFs), our findings indicate that it directly mediates the plasticity of prostate cancer cells, thereby driving NEPC progression. Specifically, in vivo and in vitro experiments confirmed that CEP55 enhances cell proliferation, migration, invasion and the expression of NEPC biomarkers in prostate cancer. Importantly, although cisplatin is the primary treatment for NEPC clinically, CEP55 has been shown to regulate cisplatin resistance through the phosphorylation of CDK1 at the tyrosine 15 (Tyr15) site. In summary, our study identifies a key gene that influences the neuroendocrine differentiation process in prostate cancer, suggesting its potential as an important therapeutic target.

神经内分泌前列腺癌（NEPC）是去势抵抗性前列腺癌（CRPC）的一种侵袭性亚型，对目前几乎所有的治疗方法都具有典型的抗性。在这项研究中，单细胞RNA测序（scRNA-seq）和数据集分析发现，中心体蛋白55 （CEP55）是激素敏感性前列腺癌（HSPC）向CRPC转化并最终向NEPC转化的关键因素。随后的生物信息学分析和临床样本验证表明，与HSPC和CRPC相比，CEP55在NEPC组织中显著上调。此外，虽然CEP55与免疫微环境或癌症相关成纤维细胞（CAFs）没有显著关联，但我们的研究结果表明，它直接介导前列腺癌细胞的可塑性，从而推动NEPC的进展。具体而言，体内和体外实验证实，CEP55可增强前列腺癌细胞的增殖、迁移、侵袭以及NEPC生物标志物的表达。重要的是，虽然顺铂是临床上NEPC的主要治疗方法，但CEP55已被证明通过酪氨酸15 （Tyr15）位点CDK1的磷酸化来调节顺铂耐药性。总之，我们的研究确定了一个影响前列腺癌神经内分泌分化过程的关键基因，表明其可能是一个重要的治疗靶点。

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引用次数: 0

Emerging risk factors and the role of gut microbiota in immunomodulation and therapeutic implications in colorectal cancer 新出现的危险因素和肠道菌群在结直肠癌免疫调节和治疗意义中的作用

IF 2.8

Cancer pathogenesis and therapy

Pub Date : 2025-07-05 DOI: 10.1016/j.cpt.2025.06.007

Sonakshi Modeel , Sneha Siwach , Padma Dolkar , Meenu Chaurasia , Pankaj Yadav , Apoorva Atri , Aarzoo Yadav , Tarana Negi , Ram Krishan Negi

The pathophysiology of many ailments, including neurological, gastrointestinal, and metabolic problems, is well known to be influenced by intestinal dysbiosis. Clinical research has provided evidence suggesting a strong correlation between dysbiosis of the gut microbiome and colorectal cancer (CRC) development. The active reprogramming of metabolic pathways to boost glycolysis, fatty acid production, lipogenesis, and glutaminolysis constitutes a major metabolic shift in cancer development, including CRC. The complex combination of different factors leads to CRC, making it an environmental disease. These factors include food and lifestyle choices, genetics and family history, age, underlying intestinal diseases, and dysbiosis of the gut microbiota. One of the primary risk factors for carcinoma development is diet, which impacts an individual’s gut microbiome. In addition to impacting CRC formation, the gut microbiome also has immunomodulatory effects, including various immunological interactions and the underlying mechanisms governing them. Microbial interactions in CRC have been extensively studied, yet numerous unresolved queries exist on how gut bacteria can influence treatment. It is possible to perform microbiome-driven immunotherapies focusing on probiotics, prebiotics, and synbiotics. However, large-scale treatment utilization in CRC patients is limited by several issues, including variations in the microbial makeup of each patient’s gut and a lack of established methods. The study highlights the impact of several risk factors, including dysbiosis of the gut microbiome and different approaches to halting and treating CRC progression with a focus on diet changes and modulation of the gut flora. Given the foregoing, we propose that if research gaps are addressed and immunotherapy is paired with microbial interventions, microbiota-based therapeutics could potentially impede the growth of tumors and treat CRC.

众所周知，许多疾病的病理生理学，包括神经、胃肠和代谢问题，都受到肠道生态失调的影响。临床研究提供的证据表明，肠道微生物群失调与结直肠癌（CRC）的发展之间存在很强的相关性。代谢途径的活性重编程促进糖酵解、脂肪酸产生、脂肪生成和谷氨酰胺解，构成了包括结直肠癌在内的癌症发展的主要代谢转变。不同因素的复杂组合导致结直肠癌，使其成为一种环境疾病。这些因素包括食物和生活方式的选择、遗传和家族史、年龄、潜在的肠道疾病和肠道微生物群的生态失调。癌症发展的主要危险因素之一是饮食，它会影响个体的肠道微生物群。除了影响结直肠癌的形成外，肠道微生物组还具有免疫调节作用，包括各种免疫相互作用及其控制机制。微生物在结直肠癌中的相互作用已被广泛研究，但关于肠道细菌如何影响治疗存在许多未解决的问题。以益生菌、益生元和合成菌为重点的微生物组驱动免疫疗法是可能的。然而，CRC患者的大规模治疗利用受到几个问题的限制，包括每个患者肠道微生物组成的变化和缺乏既定的方法。该研究强调了几个风险因素的影响，包括肠道微生物群的生态失调，以及以饮食改变和肠道菌群调节为重点的阻止和治疗结直肠癌进展的不同方法。鉴于上述情况，我们建议，如果研究空白得到解决，免疫治疗与微生物干预相结合，基于微生物群的治疗可能会阻碍肿瘤的生长并治疗结直肠癌。

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引用次数: 0

Chemoresistance: The hidden barrier in cancer treatment 化疗耐药：癌症治疗中的隐性屏障

IF 2.8

Cancer pathogenesis and therapy

Pub Date : 2025-07-05 DOI: 10.1016/j.cpt.2025.07.001

Vivek Kumar Dhiman , Manju Kumari , Devendra Singh

Despite significant advances in cancer diagnosis and therapy, the global burden of cancer continues to escalate, characterized by increasing incidence and mortality rates. A problem for successful treatment is chemoresistance, which undermines the effectiveness of traditional and targeted treatments. This review synthesizes emerging therapeutic strategies, including targeted agents, combinatorial regimens, and advances in precision medicine, with a focus on improving clinical outcomes. Integrating the latest understanding from molecular biology, genomics, and pharmacology emphasizes new paths to overcoming resistance. Particular attention is focused on the roles played by exosomes, metabolic reprogramming, and the tumour microenvironment in facilitating drug resistance, as well as promising approaches to counteract these mechanisms and improve therapeutic responsiveness.

尽管在癌症诊断和治疗方面取得了重大进展，但全球癌症负担继续加重，其特点是发病率和死亡率不断上升。成功治疗的一个问题是化疗耐药性，它破坏了传统和靶向治疗的有效性。这篇综述综合了新兴的治疗策略，包括靶向药物、联合方案和精准医学的进展，重点是改善临床结果。整合分子生物学、基因组学和药理学的最新认识，强调克服耐药性的新途径。特别关注外泌体、代谢重编程和肿瘤微环境在促进耐药中的作用，以及对抗这些机制和提高治疗反应性的有希望的方法。

引用次数: 0

Weight management in overweight or obesity: Implications for cancer pathogenesis and prognosis 超重或肥胖的体重管理：对癌症发病机制和预后的影响

Cancer pathogenesis and therapy

Pub Date : 2025-07-01 DOI: 10.1016/j.cpt.2025.05.001

Yue Wang , Haitao Niu , Peng Lyu, Bing Liu, Junmin Wei

引用次数: 0

An overview of randomized phase III clinical trials of cancer nanomedicines 肿瘤纳米药物随机III期临床试验综述

Cancer pathogenesis and therapy

Pub Date : 2025-07-01 DOI: 10.1016/j.cpt.2024.10.001

Micael N. Melo , Ricardo G. Amaral , Lucas R. Melo de Andrade , Patricia Severino , Cristina Blanco-Llamero , Luciana N. Andrade , Eliana B. Souto

Background

Cancer therapy has undergone significant advances in recent decades attributed to personalized medicine and targeted drug delivery. Among the promising approaches, the use of nano-based delivery systems has become a relevant approach capable of improving treatment by releasing antineoplastic drugs at the target site, improving therapeutic efficacy, minimizing cytotoxicity in healthy tissues, and ultimately, reducing the intensity of adverse effects of chemotherapy. This study prospectively evaluated the impact of formulating anti-neoplastic drugs as nanomedicines on clinical response, overall survival, safety, and quality of life of cancer patients, based on the outcomes of randomized clinical trials.

Methods

A literature review was carried out by systematically searching the PubMed/MEDical Literature Analysis and Retrieval System Online (MEDLINE), Excerpta Medica Database (EMBASE), and Latin American and Caribbean Health Sciences Literature (LILACS) databases for phase III clinical trials, comparing nanomedicines with conventional therapies for the treatment of various cancer types.

Results

The nanomedicines analyzed were those that are approved and used in Brazil, considering the country's emerging market for advanced cancer treatments. From a total of 303 articles found, 26 articles were selected for systematic review. Studies showed that PEGylated l-asparaginase achieved a similar therapeutic effect to that of l-asparaginase, with fewer applications due to its longer half-life. Paclitaxel bound to albumin improved therapeutic efficacy as well as reduced infusion time and solvent-related toxicity of the conventional paclitaxel formulation. PEGylated liposomal doxorubicin showed better pharmacokinetics, reduced cardiotoxicity, and improved quality of life in cancer patients compared to that of free doxorubicin.

Conclusions

This study reinforces the scientific evidence of the added value of nanomedicines to improve therapeutic efficacy and reduce toxicity in patients under chemotherapy.

近几十年来，由于个性化医疗和靶向给药，癌症治疗取得了重大进展。在这些有前景的方法中，使用纳米为基础的递送系统已经成为一种相关的方法，能够通过在靶点释放抗肿瘤药物来改善治疗，提高治疗效果，最小化健康组织中的细胞毒性，并最终降低化疗不良反应的强度。本研究基于随机临床试验的结果，前瞻性地评估了抗肿瘤药物作为纳米药物对癌症患者临床反应、总体生存期、安全性和生活质量的影响。方法系统检索PubMed/MEDical literature Analysis and Retrieval System Online （MEDLINE）、abstracts Medica Database （EMBASE）和Latin American and Caribbean Health Sciences literature （LILACS）数据库进行III期临床试验的文献综述，比较纳米药物与常规疗法治疗不同类型癌症的疗效。考虑到巴西是一个新兴的晚期癌症治疗市场，所分析的纳米药物是那些在巴西获得批准和使用的药物。从共发现的303篇文献中，选择26篇进行系统评价。研究表明，聚乙二醇化l-天冬酰胺酶与l-天冬酰胺酶具有相似的治疗效果，但由于其半衰期较长，应用较少。与传统紫杉醇制剂相比，紫杉醇与白蛋白结合提高了治疗效果，减少了输注时间和溶剂相关毒性。与游离阿霉素相比，聚乙二醇化脂质体阿霉素在癌症患者中表现出更好的药代动力学，降低心脏毒性，改善生活质量。结论本研究为纳米药物在化疗患者中提高疗效、降低毒副作用的附加价值提供了科学依据。

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引用次数: 0